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Biomedical subjects

C Picado

Publications and source records attributed to C Picado.

At least 19 recordsLinked to original sources
PubMed1992

Early and late-phase asthmatic reactions: a hypothesis.

Why might a foreign particle, exercise or fog inhalation precipitate two asthmatic reactions? It is reasonable to suspect that asthmatic patients develop two reactions because healthy subjects may also develop two physiological responses to the same stimuli. This suggestion is supported by the observation that living things have developed adaptative systems to confront either sudden or persistent changes in the environment or within the internal milieu. The results of several studies suggest that the early phase response (EPR) usually involves cells which are normal residents of the respiratory epithelium (mast cells) and pre-formed substances (histamine), whereas cells participating in the late phase reaction (LPR) are recruited from the circulation (eosinophils, basophils and T cells). Up to now most of the studies of the EPR and LPR have been addressed to detecting a cell or metabolite abnormality. This simplistic approach would probably not improve the knowledge of the mechanisms involved in asthmatic responses. Since the presence of isolated or dual responses seems to depend on the intensity and duration of the stimuli it is reasonable to suspect that EPR and LPR are the result of an excessive adaptative response of the bodies of asthmatics to sudden and prolonged/strong stimuli, respectively.

Acute Disease↗
PubMed1992

Sputum sol phase proteins and elastase activity in patients with clinically stable bronchiectasis.

BACKGROUND: Inflammatory and proteolytic activity occurs in sputum from patients with stable purulent bronchiectasis and has been proposed as the main pathogenetic mechanism of the disease. This study was designed to define further the role of inflammation and proteolysis in bronchiectasis. METHODS: Neutrophil elastase activity, sputum concentrations of the serum derived inhibitors alpha 1 antiproteinase and alpha 2 macroglobulin, and the sputum to serum ratios of albumin and C reactive protein concentration were measured in 26 patients with bronchiectasis. RESULTS: Free elastase activity was found in 15 sputum samples. A trend to higher proteolytic and inflammatory activity was found between mucoid and purulent sputum samples, suggesting that inflammatory and proteolytic activities are related to the macroscopic degree of purulence. Purulent sputum had a high sputum to serum ratio of C reactive protein, suggesting local production or active transport of this protein into bronchial secretions. C reactive protein was more sensitive than albumin in detecting a higher degree of inflammation in elastase positive samples. CONCLUSION: The finding of greater concentrations of alpha 2 macroglobulin in purulent and elastase positive samples than in mucopurulent, mucoid and elastase negative sputum samples suggests that this inhibitor may have a role in the proteolysis-antiproteolysis balance in bronchial secretions.

Albumins↗
PubMed1992

Platelet kinetics in asthmatic patients with and without aspirin intolerance.

BACKGROUND: A reduced platelet survival time has been described in asthmatic patients. There is also good evidence that platelets are involved in aspirin induced asthma. Since aspirin intolerant patients usually suffer from an active disease and often require anti-inflammatory treatment, it has been suggested that platelet survival time may be shorter in aspirin intolerant asthmatic subjects than in aspirin tolerant subjects. The objective of this study was to investigate this hypothesis. METHODS: Thirteen asthmatic subjects (six aspirin tolerant and seven aspirin intolerant) in a stable clinical condition and ten healthy subjects were studied. Platelet kinetics and survival time were measured with indium-111 labelled autologous platelets. RESULTS: Mean (SD) platelet sequestration ratios in the spleen and liver were lower in asthmatic (2.3 (0.9) and 0.6 (0.2) respectively) than in healthy subjects (3.2 (0.7) and 1.1 (0.4) respectively). However, mean (SD) platelet survival time in asthmatic subjects (8 (2.7) days) did not differ from that in healthy subjects (7.6 (1.1) days). No differences were observed in platelet kinetics between aspirin tolerant and aspirin intolerant patients. CONCLUSIONS: These results suggest the existence of an active non-splenic pool of platelets in patients with asthma. However, they failed to show platelet kinetic differences among asthmatic subjects with and without aspirin intolerance and do not support previous studies suggesting an altered platelet survival in stable asthma.

Adult↗
PubMed1992

Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients.

Although the mechanism of aspirin-induced asthma and rhinitis is unknown, it has been suggested that adverse nasal and bronchial reactions are caused by an increased production of lipoxygenase products. In examining this hypothesis we have measured the release of peptide leukotrienes (PeptLTs), 15-HETE, and prostaglandins in nasal fluids obtained by nasal lavages after instillation of acetylsalycilic acid (ASA) and placebo (saline). Ten ASA-sensitive asthmatics, 10 ASA-insensitive asthmatics, and seven healthy subjects were challenged in a double-blind study with normal saline and 12 mg of ASA. Twelve mg were administered based on the results of a previous study that showed that this dose caused minor to moderate symptoms in ASA-sensitive patients. PeptLTs, LTB4, 15-HETE, PGE2, PGF2 alpha, and PGD2 were measured by radioimmunoassay methods. Significant levels of PeptLTs were detected in sensitive asthmatic patients 60 min after nasal challenge. This change was associated with a significant increase in symptoms. No increase in PeptLTs levels were found, however, in either insensitive patients or healthy subjects. Inhibition of PGE2 and PGF2 alpha release was detected in the three groups after ASA administration. ASA also inhibited PGD2 release in insensitive asthmatic patients but not in both sensitive patients and healthy subjects. These results suggest that an abnormal release of PeptLTs in ASA-sensitive asthmatic patients contributes to nasal and bronchial adverse reactions. The lack of effects on PGD2 release suggests that mast cells from ASA-insensitive patients are more sensitive to ASA than those from sensitive asthmatic patients and healthy subjects.

Administration, Intranasal↗
PubMed1991

Ototoxic reaction to erythromycin.

We report a case of bilateral hearing loss in a patient treated with intravenous erythromycin lactobionate. The ototoxic reaction occurred despite the patient's having normal renal and hepatic function and the fact that serum erythromycin levels were within the predicted normal range. In addition to hearing loss, a marked labyrinthic hyporreflexia was also observed. Hearing loss improved after the treatment was discontinued, but labyrinthic abnormalities persisted suggesting that erythromycin had caused a permanent vestibular damage.

Erythromycin↗
PubMed1991

In vivo release of 15-HETE and other arachidonic acid metabolites in nasal secretions during early allergic reactions.

The purpose of this study is to examine the "in vivo" release of 15-HETE and other arachidonic acid metabolites in nasal secretions following a challenge with "Dermatophagoides Pteronyssinus" in patients with allergic rhinitis and non-allergic controls. In addition, we examine the effects of a membrane stabilizer, such as sodium cromoglycate, on these metabolites. Thirteen allergic subjects and seven healthy controls are studied. 15-HETE, peptide leukotrienes, LTB4, PGD2, PGE2 and PGF2 alpha levels are evaluated before and after nasal challenge in sodium cromoglycate treated and untreated subjects. This study provides "in vivo" evidence that the pathophysiological responses to nasal antigen challenge could be related to the release of 15-HETE as well as other arachidonic acid metabolites, mainly arising from the lipoxygenase pathway.

Adolescent↗
PubMed1991

Identification of mast cells in bronchoalveolar lavage fluid. Comparison between different fixation and staining methods.

The present study was carried out to compare the effectiveness of different fixation and staining methods in the identification of mast cells obtained by bronchoalveolar lavage from patients with interstitial lung diseases. Cell preparations were fixed with formaldehyde or methanol. Mast cells were identified by metachromatic staining with May Grünwald Giemsa, Toluidine blue or Gallamine blue Giemsa. After formaldehyde fixation only a few mast cells were identified, regardless of the stain method used. In contrast, a significantly higher number of mast cells were observed after methanol fixation. Using this fixative, Toluidine blue stain showed a higher number of mast cells than May Grünwald Giemsa. However, there was no difference between Toluidine and Gallamine blue Giemsa in the number of cells observed. The easy identification of mast cells after staining with toluidine, combined with its easy application, suggest that Toluidine blue stain after methanol fixation is the most useful method for determining the presence of mast cells in lavage fluid.

Bronchoalveolar Lavage Fluid↗
PubMed1991

Effect of negative pressure ventilation on arterial blood gas pressures and inspiratory muscle strength during an exacerbation of chronic obstructive lung disease.

The effects of intermittent negative pressure ventilation have been studied in 20 patients with chronic obstructive pulmonary disease during an exacerbation of their disease. Measurements of arterial blood gas tensions and maximal inspiratory pressure (MIP) were performed before and after six hours of negative pressure ventilation or standard treatment (control day) given in random order on two consecutive days. After negative pressure ventilation the mean (SD) value of MIP increased from 68.1 (21.5) to 74.8 (20) cm H2O;* arterial oxygen tension (PaCO2) fell from 60.6 (12.2) to 50.9 (8.9) mm Hg* but PaO2 changed little (from 48.4 (7.4) to 47.6 (8.2) mm Hg). There were no significant changes on the control day in arterial blood gas tensions (PaO2 47.8 (8.1) and 48.9 (9.4) and Paco2 59.8 (10.9) and 57.5 (8.06) mm Hg) or in MIP (69.4 (22.4) and 70.9 (22.9) cm H2O). Six patients tolerated negative pressure ventilation poorly and these patients showed less improvement after negative pressure ventilation. Our results suggest that intermittent negative pressure ventilation can increase alveolar ventilation in patients with an exacerbation of chronic obstructive lung disease, particularly in those who tolerate the procedure well. Most subjects showed a fall in PaCO2 and an increase in MIP. The fact that PaO2 was unchanged despite the fall in PaCO2 suggests that gas exchange may deteriorate with negative pressure ventilation in these patients.

Aged↗
PubMed1991

Vertebral fractures in steroid dependent asthma and involutional osteoporosis: a comparative study.

BACKGROUND: Reduced bone mass predisposes patients to the development of vertebral fractures. Measurement of bone mass by non-invasive methods is used to detect patients with involutional osteoporosis at risk from fractures. These methods have not been assessed in patients with steroid dependent osteoporosis. The objective of this study was to assess the value of a predictive fracture threshold value of bone density in patients with steroid dependent asthma. METHODS: Three groups of patients were studied. Group 1 (67 patients) had steroid dependent asthma (mean daily dose of prednisone 11.7 mg) and no vertebral fractures, group 2 (32 patients) had steroid dependent asthma (mean daily dose of prednisone 12 mg) and vertebral fractures, and group 3 (55 patients) were not taking steroids but had involutional osteoporosis and a recent non-traumatic vertebral fracture. Bone mineral density was measured by dual photon absorptiometry and vertebral fractures by radiography of the lumbar spine. A fracture threshold was determined in the two groups with fractures as the 90th percentile of the mean bone mineral density measured in the lumbar spine. RESULTS: Bone mineral density was significantly higher in the steroid dependent group with fractures (group 2) than in group 3 patients, who had involutional osteoporosis and fractures (0.946 (0.18) g/cm2 v 0.830 (0.16) g/cm2). The fracture threshold value was therefore higher for patients with steroid related vertebral fractures (group 2, 1.173 g/cm2) than for those with involutional osteoporosis (group 3, 0.979 g/cm2). Vertebral fractures were more likely to occur in steroid dependent asthmatic patients with bone density above the fracture threshold value (obtained from subjects with involutional osteoporosis) than in subjects in group 3 (34% v 9%). CONCLUSION: Vertebral fractures occur in patients treated with steroids in the presence of higher bone mineral density than is the case with patients with involutional osteoporosis. The findings suggests that the assessment of the efficacy of preventive treatment requires measurement of bone mineral density and radiology.

Adult↗
PubMed1991

[Skill in the handling of aerosols by health care personnel].

Aerosol bronchodilators are extensively used in bronchial asthma treatment and other obstructive pulmonary diseases. Its therapeutic efficacy is closely related to a correct administration technique. We present the results obtained in a prospective study on the skill in the use of the health care professionals in our hospital. A total of 127 physicians and nurses were interviewed, being 110 finally included in the study. Only 22.7% of them used the aerosol correctly and we did not find significant differences between the three groups into which we divided the study (Staff physicians, Residents, and nurses). The most frequently found mistakes were not maintaining as correct apnea after inhalation (62.7%) and not shaking the aerosol before use (48.2%). Up to a 57.2% of those interviewed made two or more of the evaluated mistakes. We conclude that although aerosol bronchodilators and corticoids are extensively prescribed, the lack of knowledge about their correct use by health care professionals is very high, and this could contribute to their misuse by patients under their care.

Adult↗
PubMed1991

Intestinal calcium absorption and parathyroid hormone secretion in asthmatic patients on prolonged oral or inhaled steroid treatment.

A secondary hyperparathyroidism resulting from decreased intestinal calcium (Ca) absorption has been proposed as a contributory factor to glucocorticoid-induced osteoporosis. Inhaled steroids do not usually suppress adrenal gland function unless daily doses above 1,500 microgram are used. A recent study, however, has shown a reduced total body calcium in patients on regular beclomethasone treatment. In theory, osteopenia in these patients could be due to a direct effect of inhaled steroids on bone or due to an impaired intestinal calcium absorption. In this study, Ca absorption and parathyroid hormone (PTH) secretion were evaluated in three groups: 1) asthmatics on continuous oral and inhaled steroid treatment (11.3 +/- 4.4, range 5-33.5 mg.day-1 prednisone and 660 +/- 265, range 400-1,600 microgram.day-1 beclomethasone, respectively); 2) asthmatics on regular beclomethasone therapy (585 +/- 210, range 400-1,200 microgram.day-1); and 3) healthy subjects. The prevalence of vertebral fractures was evaluated by a spinal X-ray. No differences were found in either Ca absorption or PTH serum levels between asthmatics and healthy subjects (analysis of variance-ANOVA). Vertebral fractures were significantly more frequent in patients from group 1 (14 of 25) than in those from group 2 (2 or 25). We conclude that both prolonged oral steroid treatment and inhaled steroids, at doses lower than 1,600 microgram.day-1 do not cause Ca malabsorption, and that hyperparathyroidism does not contribute to osteoporosis in these patients.

Administration, Inhalation↗
PubMed1990

Simultaneous reversed-phase extraction of lipoxygenase and cyclooxygenase metabolites of arachidonic acid in nasal secretions: methodological aspects.

An improved analytical method for the simultaneous solid-phase extraction of arachidonic acid metabolites in biological samples is described. The major aim of the work was to define the cause of the different recoveries reported in the literature for leukotrienes and hydroxyeicosatetraenoic acids. We used nasal lavages to carry out a comparative study of solid-phase extraction parameters of practical importance in securing good recoveries of leukotrienes and hydroxyeicosatetraenoic acids from biological samples. We evaluated the influence of the pH of the sample, the pH of the water used to wash the extraction cartridge before elution of the adsorbed analytes, the comparative behaviour of commercially available octadecyl adsorbents and the influence of the concentration-evaporation step on final recoveries. Data thus obtained show that there is no significant difference in results when the samples and the water used to wash the cartridge before analyte elution are adjusted to pH values ranging between 4.0 and 7.4. Below pH 4.0, losses may be significant. Furthermore, recoveries can be very much dependent on the type of solid-phase cartridge material and on the eluent evaporation method, especially with regard to aqueous phase removal.

Arachidonic Acid↗
PubMed1990

Recovery of nasal prostaglandin production after inhibition by aspirin.

We have investigated the duration of the inhibitory effects of aspirin in eight healthy volunteers after oral administration of a single 500 mg dose. Prostaglandin E2, D2 and leukotriene C4 levels in nasal lavage fluid were measured by radioimmunoassay without purification by high performance liquid chromatography. The inhibitory effects of aspirin on eicosanoid synthesis were maximum between 1 h to 24 h, showing total recovery within 3-5 days. LTC4 synthesis was not modified by aspirin.

Adult↗
PubMed1990

Respiratory and skeletal muscle function in steroid-dependent bronchial asthma.

Respiratory and skeletal (deltoid) muscle strength were evaluated in 34 oral steroid-dependent asthmatics by use of maximal inspiratory and expiratory pressures and a myometer. The patients were compared to age- and sex-matched asthmatics who had never been on continuous oral steroid treatment. Endurance time was also studied in ten steroid-dependent asthmatics and ten controls using a pressure threshold breathing device. Nutritional status was assessed from body weight, midarm circumference, triceps skinfold (TSF), prealbumin, albumin, and total protein. An open biopsy from deltoid muscle was taken from nine steroid-dependent asthmatics and the diameter of type 1 and type 2 fibers was measured by a morphometric study. No differences were found between study and control groups either in respiratory and skeletal muscle strength or in endurance time. Steroid-dependent asthmatics showed a decrease in TSF, total protein, albumin, and potassium serum levels when compared with the control group but differences were not statistically significant after Bonferroni's adjustment for multiple comparison studies. Transversal diameter of type 2 fibers was significantly correlated with the percentage of ideal weight (r = 0.75 p less than 0.05), but not with average daily dose of steroids nor with the length of steroid treatment. Our results support the clinical impression that steroids, at the doses usually administered in chronic severe asthma, do not cause muscular weakness. We also found that malnutrition rather than corticosteroids is the most important contributory factor to type 2 muscle fiber atrophy in steroid-dependent asthma.

Adult↗